Project description:ACTH is known to be secreted from pituitary cortictropes after CRH and Il-6 stimulation. Recenetly it was proven that eNampt also stimulates ACTH secretion from rat pituitary gland. We used microarrays to detail the global programme of gene expression in isolated rat pituitary corticotropes, 24h after administration of eNampt, CRH and Il-6.
Project description:We generated a single nuclei RNA-seq (snRNA-seq) dataset derived from the postnatal hypothalamus of CRH-IRESCre (CRH-Cre) mice using a retrograde Connect-seq approach.
Project description:Here we translationally profiled the transcriptome of Crh-expressing neurons (Crh neurons) within the CeA following fear conditioning (FC) and fear extinction (EXT) in mice using translating ribosome affinity purification (TRAP) followed by RNA sequencing. A tone alone group (TA) was used as a control group.
Project description:Rationale: A previous transcriptome meta-analysis revealed significantly lower levels of corticotropin-releasing hormone (CRH) mRNA in corticolimbic brain regions in major depressive disorder (MDD) subjects. Rodent studies show that cortical CRH is mostly expressed in GABAergic neurons; however, the characteristic features of CRH+ cells in human brain cortex and their association with MDD are largely unknown. Methods: Subgenual anterior cingulate cortex (sgACC) of human subjects without brain disorders were labeled using fluorescent in situ hybridization (FISH) for CRH and markers of excitatory (SLC17A7), inhibitory (GAD1) neurons, as well as markers of other interneuron subpopulations (PVALB, SST, VIP). MDD-associated changes in CRH+ cell density and cellular CRH expression (n=6/group) were analyzed. RNA-sequencing was performed on sgACC CRH+ neurons from comparison and MDD subjects (n=6/group), and analyzed for group differences. Results: About 80% of CRH+ cells were GABAergic and 17.5% were glutamatergic. CRH+ GABAergic neurons co-expressed VIP (52%), SST (7%), or PVALB (7%). MDD subjects displayed lower CRH mRNA levels in GABAergic neurons relative to comparison subjects without changes in cell density. CRH+ neurons show transcriptomic profile suggesting lower excitability and less GABA release and reuptake. Further analyses suggested that these molecular changes are not mediated by altered glucocorticoid feedback and potentially occur downstream for a common modulator of neurotrophic function. Summary: CRH+ cells in human sgACC are a heterogeneous population of GABAergic neurons, although largely co-expressing VIP. MDD is associated with reduced markers of inhibitory function of CRH+ neurons.
Project description:MCF7 cells were stimulated with vehicle or 100nM corticotropin releasing hormone (CRH) for 24h. The effect of CRH on the expression of genes relevant to estrogen signalling was investigated by using the Human Estrogen Receptor Signaling RT² Profiler™ PCR Array (SABioscience Corp).
Project description:MCF7 cells were stimulated with vehicle or 100nM corticotropin releasing hormone (CRH) for 24h. The effect of CRH on the expression of genes relevant to estrogen signalling was investigated by using the Human Estrogen Receptor Signaling RTM-BM-2 ProfilerM-bM-^DM-" PCR Array (SABioscience Corp). qPCR gene expression profiling. MCF7 cells were treated separately in triplicate. Equal amount total RNA was processed further for gene expression analysis.
Project description:We report genome-wide gene expression changes in olfactory bulb cells, in the context of low, wild-type or high levels of local CRH signaling by local interneurons onto adult-born CRHR1+ granule neurons. To test the gene expression changes associated with altered local CRH signaling, we utilize the following animal models: CRHR1-/- mice whose bulbs were infected with a control AAV-flex-EGFP virus = low local CRH signaling, CRHR1-Cre mice whose bulbs were infected with AAV-flex-EGFP = pseudo-wild-type local CRH signaling, and CRHR1-Cre mice whose bulbs were infected with AAV-flex-(CA)CRHR1, which is a constitutively active variant of CRHR1 = high local CRH signaling. We find that, in response to changes in local CRH signaling in the bulb, the largest ontological category of transcription changes in the bulb that occurs reciprocally between low and high levels of CRH signaling are gene regulatory factors. To test the contributions of one of these factors, POU6f1, we perform loss- and gain-of-function analysis. We show that CRHR1 activation results in transcriptional activation of POU6f1 and that POU6f1 in turn influences synaptogenesis and dendritic patterning of adult-born neurons and olfactory circuit behavior.
Project description:As the Crh-system and the HPA-axis are known to be crucially involved in the onset, development and maintainance of psychiatric disorders like anxiety and depression and regulate the behavioural and endocrine stress responses the further analysis of Crhr1-dependent signaling cascades is essential to understand the molecular mechanisms behind these psychiatric diseases. In this project, new candidate genes involved in Crhr1-dependent signaling cascades were dissected in the cell line model of AtT-20 cells by transcriptional profiling of mouse pituitary corticotroph cells comparing control untreated AtT-20 cells with AtT-20 cells treated with 100 nM Crh at 1, 3, 6, 12 and 24 hours. Keywords: time course, treatment response Two condition experiment: untreated vs. 100 nM Crh treated AtT-20 cells with a time curve of 1, 3, 6, 12, 24 hours. Technical replicates: 6 for each time point, including dye-swap each with 3 replicates